Neuroscientists have become used to a number of “facts” about the human brain: It has 100 billion neurons and 10- to 50-fold more glial cells; it is the largest-than-expected for its body among primates and mammals in general, and therefore the most cognitively able; it consumes an outstanding 20% of the total body energy budget despite representing only 2% of body mass because of an increased metabolic need of its neurons; and it is endowed with an overdeveloped cerebral cortex, the largest compared with brain size. These facts led to the widespread notion that the human brain is literally extraordinary: an outlier among mammalian brains, defying evolutionary rules that apply to other species, with a uniqueness seemingly necessary to justify the superior cognitive abilities of humans over mammals with even larger brains. These facts, with deep implications for neurophysiology and evolutionary biology, are not grounded on solid evidence or sound assumptions, however. The recent development of a method that allows rapid and reliable quantification of the numbers of cells that compose the whole brain has provided a means to verify these facts. With 86 billion neurons and just as many nonneuronal cells, the human brain is a scaled-up primate brain in its cellular composition and metabolic cost, with a relatively enlarged cerebral cortex that does not have a relatively larger number of brain neurons yet is remarkable in its cognitive abilities and metabolism simply because of its extremely large number of neurons.

By simulating 25,000 generations of evolution within computers, Cornell University engineering and robotics researchers have discovered why biological networks tend to be organized as modules – a finding that will lead to a deeper understanding of the evolution of complexity. The new insight also will help evolve artificial intelligence, so robot brains can acquire the grace and cunning of animals. From brains to gene regulatory networks, many biological entities are organized into modules – dense clusters of interconnected parts within a complex network.

For decades biologists have wanted to know why humans, bacteria and other organisms evolved in a modular fashion. Like engineers, nature builds things modularly by building and combining distinct parts, but that does not explain how such modularity evolved in the first place. Renowned biologists Richard Dawkins, Günter P. Wagner, and the late Stephen Jay Gould identified the question of modularity as central to the debate over "the evolution of complexity." For years, the prevailing assumption was simply that modules evolved because entities that were modular could respond to change more quickly, and therefore had an adaptive advantage over their non-modular competitors. But that may not be enough to explain the origin of the phenomena. The team discovered that evolution produces modules not because they produce more adaptable designs, but because modular designs have fewer and shorter network connections, which are costly to build and maintain. As it turned out, it was enough to include a "cost of wiring" to make evolution favor modular architectures.

The results may help explain the near-universal presence of modularity in biological networks as diverse as neural networks – such as animal brains – and vascular networks, gene regulatory networks, protein-protein interaction networks, metabolic networks and even human-constructed networks such as the Internet. "Being able to evolve modularity will let us create more complex, sophisticated computational brains," says Clune. Says Lipson: "We've had various attempts to try to crack the modularity question in lots of different ways. This one by far is the simplest and most elegant."

For about 70 years, breeders have selected tomato varieties with uniformly light green fruit before ripening. These tomatoes then turn red evenly as they ripen, and they look nice in a supermarket display. Researchers now have pinpointed the molecular changes responsible for this “uniform ripening” trait of many modern tomatoes. But these changes, they show, also reduce the fruit's sugar content.

Ann Powell of the University of California, Davis and colleagues report that the gene at the heart of uniform ripening encodes a protein called GLK2. This protein increases the fruit's photosynthetic capacity, helping along the production of sugars and lycopene, the pigment that gives a ripe tomato its brilliant color. Breeding the tomatoes to contain the “uniform ripening” mutation disables GLK2, however. This change has the unintended effect of impairing the development of chloroplasts, the structures in plant cells that enable plants to photosynthesize. Impairing their development decreases the production of key ingredients that give tomatoes their sweetness.

Walter Tschinkel may not have solved the mystery of the fairy circles, but he can tell you that they're alive. Tens of thousands of the formations—bare patches of soil, 2 to 12 meters in diameter—freckle grasslands from southern Angola to northern South Africa, their perimeters often marked by a tall fringe of grass. Locals say they're the footprints of the gods. Scientists have thrown their hands up in the air. But now Tschinkel, a biologist at Florida State University in Tallahassee, has discovered something no one else has.

The Guardian (blog)Good and outstanding leadership: what's the difference?The Guardian (blog)An appreciative inquiry approach leads to looking at what works and building on this – rather than getting mired in the weeds of old problems.

Transposable elements are mobile strands of DNA that insert themselves into chromosomes with mostly harmful consequences. Cells try to keep them locked down, but in a new study, Brown University researchers report that aging cells lose their ability to maintain this control. The result may be a further decline in the health of senescent cells and of the aging bodies they compose.

Even in our DNA there is no refuge from rogues that prey on the elderly. Parasitic strands of genetic material called transposable elements—transposons—lurk in our chromosomes, poised to wreak genomic havoc. Cells have evolved ways to defend themselves, but in a new study, Brown University researchers describe how cells lose this ability as they age, possibly resulting in a decline in their function and health. Barbara McClintock, awarded the Nobel Prize in 1983, made the original discovery of transposons in maize. Since then scientists have found cases in which the chaos they bring can have long-term benefits by increasing genetic diversity in organisms, but in most cases the chaos degrades cell function, such as by disrupting useful genes. "The cell really is trying to keep these things quiet and keep these things repressed in its genome," said John Sedivy, professor of medical science in the Department of Molecular Biology, Cell Biology, and Biochemistry and senior author of the new study published online in the journal Aging Cell. "We seem to be barely winning this high-stakes warfare, given that these molecular parasites make up over 40 percent of our genomes." Cells try to clamp down on transposons by winding and packing transposon-rich regions of the genome around little balls of protein called nucleosomes. This confining arrangement is called heterochromatin, and the DNA that is trapped in such a tight heterochromatin prison cannot be transcribed and expressed. What the research revealed, however, is that carefully maintaining a heterochromatin prison system is a younger cell's game.

One consequence of the fundamental difference between flat surfaces and spherical surfaces, such as the Earth, is that any planar depiction of the Earth – such as a map on the wall, in an atlas, or on Google Maps – will necessarily have some distortions.

It is challenging for patients with type 1 diabetes to control their glucose levels because tight glucose control increases the incidence of hypoglycemia (dangerously low glucose levels). Insulin pump treatment, which provides a continuous predetermined subcutaneous supply of insulin, is available, but hypoglycemia still occurs.

"Hypoglycemia is feared by most patients and remains the most common adverse effect of insulin therapy," writes Ahmad Haidar, Institut de Recherches Cliniques de Montréal and McGill University, with coauthors.

The dual-hormone artificial pancreas delivers insulin and glucagon using infusion pumps based on continuous glucose sensor readings as guided by an intelligent dosing algorithm. The infusion pumps and the glucose sensors are already on the market, but the intelligent algorithm was developed by the researchers in Montreal.

New intelligent algorithms could help robots to quickly recognize and respond to human gestures. Researchers have created a computer program which recognizes human gestures quickly and accurately, and requires very little training.

Neuroscientists have become used to a number of “facts” about the human brain: It has 100 billion neurons and 10- to 50-fold more glial cells; it is the largest-than-expected for its body among primates and mammals in general, and therefore the most cognitively able; it consumes an outstanding 20% of the total body energy budget despite representing only 2% of body mass because of an increased metabolic need of its neurons; and it is endowed with an overdeveloped cerebral cortex, the largest compared with brain size. These facts led to the widespread notion that the human brain is literally extraordinary: an outlier among mammalian brains, defying evolutionary rules that apply to other species, with a uniqueness seemingly necessary to justify the superior cognitive abilities of humans over mammals with even larger brains. These facts, with deep implications for neurophysiology and evolutionary biology, are not grounded on solid evidence or sound assumptions, however. The recent development of a method that allows rapid and reliable quantification of the numbers of cells that compose the whole brain has provided a means to verify these facts. With 86 billion neurons and just as many nonneuronal cells, the human brain is a scaled-up primate brain in its cellular composition and metabolic cost, with a relatively enlarged cerebral cortex that does not have a relatively larger number of brain neurons yet is remarkable in its cognitive abilities and metabolism simply because of its extremely large number of neurons.

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